| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5546629 | Acta Pharmaceutica Sinica B | 2017 | 9 Pages |
Abstract
Evading apoptosis is a hallmark of cancer cells. How to attack the apoptotic defects, through direct inhibition of BCL-2 family proteins or by indirect regulation of other promoting survival signaling pathways, is the challenge for modern cancer therapies. Fortunately, a lot of progress has been made to meet that challenge.193
Keywords
Bcl-2 homologous antagonist killerCLLITKNHLBcl-2-interacting mediator of cell deathNIHGSK-3Bcl-xLBH3Bcl-2 homology 3SLLCMLMCLBCL-2 related ovarian killerBcl-2PI3KCDKp53 up-regulated modulator of apoptosisFDAmyeloid cell leukemiaERKBCRBH3 Interacting Domain Death AgonistBtkmitochondrial outer membrane permeabilizationBaxBADT-ALLBIKCHOPBcl-2 familyAshApoptosisCombination therapyTargeted therapyNSCLCNon-small cell lung cancerendoplasmic reticulumphosphatidylinositol-3-kinaseB-cell lymphoma 2Non-Hodgkin lymphomaSmall lymphocytic lymphomaChronic lymphocytic leukemiachronic myelogenous leukemiaNational Institutes of HealthMOMPBIMcomplete responseBcl-2-associated X proteinBAKPUMABIDBokextracellular signal-regulated kinasecyclin-dependent kinaseglycogen synthase kinase-3B-cell receptorEGFR, epidermal growth factor receptor
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Authors
Jing Deng,